| Project/Area Number |
25861421
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Urology
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HONDA Masashi 鳥取大学, 医学部・附属病院, 講師 (20362890)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | トランスポーター / グルタミン酸 / ラット / 下部尿路機能 / 膀胱内圧測定 / グルタミン酸輸送体 |
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| Outline of Final Research Achievements |
Intrathecal and intraventricular administration of nonselective glutamate transporters inhibitors were confirmed to suppress the micturition reflex in urethane anesthetized rats. We performed a similar experiment for each of the sub-type of glutamate transporters, but were difficult to determining the optimal dose in the drug affinity. It was reported that glutamic acid is an excitatory neurotransmitter in the micturition reflex and glycine is an inhibitory neurotransmitter. In synapse of central nervous system, the concentration of the glutamic acid and glycine are involved in urinary reflex. So, we used ALX5407, a selective inhibitor of glycine transporter GlyT-1, to access the effect of the micturition reflex in urethane anesthetized rats.
Intraventricular administration of ALX5407, there were no significant change in the micturition reflex. On the other hand, intrathecal administration, inhibition at GlyT-1 in the spinal level was elucidated to suppress the micturition reflex.
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